European Heart Journal (2007) 28, 25252538

doi:10.1093/eurheartj/ehm355
Expert consensus document

Universal denition of myocardial infarction

Kristian Thygesen, Joseph S. Alpert and Harvey D. White on behalf
of the Joint ESC/ACCF/AHA/WHF Task Force for the Redenition
of Myocardial Infarction
Task Force Members:
Chairpersons: Kristian Thygesen (Denmark)*, Joseph S. Alpert (USA)*, Harvey D. White (New Zealand)*
Biomarker Group: Allan S. Jaffe, Co-ordinator (USA), Fred S. Apple (USA), Marcello Galvani (Italy),
Hugo A. Katus (Germany), L. Kristin Newby (USA), Jan Ravkilde (Denmark)
ECG Group: Bernard Chaitman, Co-ordinator (USA), Peter M. Clemmensen (Denmark), Mikael Dellborg
(Sweden), Hanoch Hod (Israel), Pekka Porela (Finland)
Imaging Group: Richard Underwood, Co-ordinator (UK), Jeroen J. Bax (The Netherlands)

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George A. Beller (USA), Robert Bonow (USA), Ernst E. Van Der Wall (The Netherlands)
Intervention Group: Jean-Pierre Bassand, Co-ordinator (France), William Wijns, Co-ordinator (Belgium),
T. Bruce Ferguson (USA), Philippe G. Steg (France), Barry F. Uretsky (USA), David O. Williams (USA)
Clinical Investigation Group: Paul W. Armstrong, Co-ordinator (Canada), Elliott M. Antman (USA),
Keith A. Fox (UK), Christian W. Hamm (Germany), E. Magnus Ohman (USA), Maarten L. Simoons
(The Netherlands)
Global Perspective Group: Philip A. Poole-Wilson, Co-ordinator (UK), Enrique P. Gurnkel (Argentina),
Jose-Luis Lopez-Sendon (Spain), Prem Pais (India), Shanti Mendis (Switzerland), Jun-Ren Zhu (China)
Implementation Group: Lars C. Wallentin Co-ordinator (Sweden), Francisco Fernandez-Aviles (Spain),
Kim M. Fox (UK), Alexander N. Parkhomenko (Ukraine), Silvia G. Priori (Italy), Michal Tendera (Poland),
Liisa-Maria Voipio-Pulkki (Finland)

ESC Committee for Practice Guidelines: Alec Vahanian, Chair (France), A. John Camm (UK), Raffaele De Caterina (Italy),
Veronica Dean (France), Kenneth Dickstein (Norway), Gerasimos Filippatos (Greece), Christian Funck-Brentano (France),
Irene Hellemans (The Netherlands), Steen Dalby Kristensen (Denmark), Keith McGregor (France), Udo Sechtem (Germany),
Sigmund Silber (Germany), Michal Tendera (Poland), Petr Widimsky (Czech Republic), Jose Luis Zamorano (Spain)

Document Reviewers: Joao Morais, Review Co-ordinator (Portugal), Sorin Brener (USA), Robert Harrington (USA),
David Morrow (USA), Udo Sechtem (Germany), Michael Lim (Singapore), Marco A. Martinez-Rios (Mexico), Steve Steinhubl
(USA), Glen N. Levine (USA), W. Brian Gibler (USA), David Goff (USA), Marco Tubaro (Italy),
Darek Dudek (Poland), Nawwar Al-Attar (France)

The recommendations set forth in this report are those of the Task Force Members and do not necessarily reect the ofcial position of the American College of Cardiology.

* Corresponding authors/co-chairpersons. Professor Kristian Thygesen, Department of Medicine and Cardiology, Aarhus University Hospital, Tage Hansens, Gade 2, DK-8000
Aarhus C, Denmark. Tel: 45 89 49 76 14; fax: 45 89 49 76 19. E-mail: Kristian.Thygesen@as.aaa.dk. Professor Joseph Alpert, Department of Medicine, University of Arizona
College of Medicine, 1501 N. Campbell Ave, PO Box 245017, Tucson, AZ 85724-5017, USA. Tel: 1 520 626 6138; fax: 1 520 626 6604. E-mail: jalpert@email.arizona.edu.
Professor Harvey White, Green Lane Cardiovascular Service, Auckland City Hospital, Private Bag 92024, 1030 Auckland, New Zealand. Tel: 64 96309992; fax: 64 96309915.
E-mail: harveyw@adhb.govt.nz

Dr Shanti Mendis of the WHO participated in the task force in her personal capacity, but this does not represent WHO approval of this document at the present time.
This article has been copublished in the October II (Vol. 28 no. 20), 2007, issue of the European Heart Journal (also available on the Web site of the European Society of Cardiology at
www.escardio.org), the November 27, 2007, issue of Circulation (also available on the Web site of the American Heart Association at my.americanheart.org), and the November 27,
2007, issue of the Journal of the American College of Cardiology (also available on the Web site of the American College of Cardiology at www.acc.org).
This document was approved by the European Society of Cardiology in April 2007, the World Heart Federation in April 2007, and by the American Heart Association Science Advisory
and Coordinating Committee May 9, 2007. The European Society of Cardiology, the American College of Cardiology, the American Heart Association, and the World Heart Federation
request that this document be cited as follows: Thygesen K, Alpert JS, White HD; Joint ESC/ACCF/AHA/WHF Task Force for the Redenition of Myocardial Infarction. Universal denition
of myocardial infarction. Eur Heart J 2007;28:25252538.
The content of this European Society of Cardiology (ESC) document has been published for personal and educational use only. No commercial use is authorized. No part of the document
may be translated or reproduced in any form without written permission from the ESC. Permission can be obtained upon submission of a written request to Oxford University Press,
the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC.
Disclaimer. The document represents the views of the ESC, which were arrived at after careful consideration of the available evidence at the time they were written. Health
professionals are encouraged to take them fully into account when exercising their clinical judgement. The document does not, however, override the individual responsibility of
health professionals to make appropriate decisions in the circumstances of the individual patients, in consultation with that patient, and where appropriate and necessary the patients
guardian or carer. It is also the health professionals responsibility to verify the rules and regulations applicable to drugs and devices at the time of prescription.

& The European Society of Cardiology, the American College of Cardiology Foundation, the American Heart Association, and the World Heart
Federation 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
2526
Introduction
Myocardial infarction is a major cause of death and disability
worldwide. Coronary atherosclerosis is a chronic disease
with stable and unstable periods. During unstable periods
with activated inammation in the vascular wall, patients
may develop a myocardial infarction. Myocardial infarction
may be a minor event in a lifelong chronic disease, it may
even go undetected, but it may also be a major catastrophic
event leading to sudden death or severe haemodynamic
deterioration. A myocardial infarction may be the rst mani-
festation of coronary artery disease, or it may occur, repeat-
edly, in patients with established disease. Information on
myocardial infarction attack rates can provide useful data
K. Thygesen et al.
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regarding the burden of coronary artery disease within and
across populations, especially if standardized data are col-
lected in a manner that demonstrates the distinction
between incident and recurrent events. From the epidemio-
logical point of view, the incidence of myocardial infarction
in a population can be used as a proxy for the prevalence of
coronary artery disease in that population. Furthermore, the
term myocardial infarction has major psychological and
legal implications for the individual and society. It is an indi-
cator of one of the leading health problems in the world,
and it is an outcome measure in clinical trials and observa-
tional studies. With these perspectives, myocardial infarc-
tion may be dened from a number of different clinical,
Universal denition of myocardial infarction
electrocardiographic, biochemical, imaging, and pathologi-
cal characteristics.
In the past, a general consensus existed for the clinical syn-
drome designated as myocardial infarction. In studies of
disease prevalence, the World Health Organization (WHO)
dened myocardial infarction from symptoms, ECG abnorm-
alities, and enzymes. However, the development of more
sensitive and specic serological biomarkers and precise
imaging techniques allows detection of ever smaller
amounts of myocardial necrosis. Accordingly, current clinical
practice, health care delivery systems, as well as epidemiol-
ogy and clinical trials all require a more precise denition of
myocardial infarction and a re-evaluation of previous de-
nitions of this condition.
It should be appreciated that over the years, while more
specic biomarkers of myocardial necrosis became avail-
able, the accuracy of detecting myocardial infarction
has changed. Such changes occurred when glutamine-
oxaloacetic transaminase (GOT) was replaced by lactate
dehydrogenase (LDH) and later by creatine kinase (CK) and
the MB fraction of CK, i.e. CKMB activity and CKMB mass.
Current, more specic, and sensitive biomarkers and
imaging methods to detect myocardial infarction are
further renements in this evolution.
In response to the issues posed by an alteration in our
ability to identify myocardial infarction, the European
Society of Cardiology (ESC) and the American College of Car-
diology (ACC) convened a consensus conference in 1999 in
order to re-examine jointly the denition of myocardial
infarction (published in the year 2000 in the European
Heart Journal and Journal of the American College of Cardi-
ology 1). The scientic and societal implications of an altered
denition for myocardial infarction were examined from
seven points of view: pathological, biochemical, electro-
cardiographic, imaging, clinical trials, epidemiological, and
public policy. It became apparent from the deliberations of
the former consensus committee that the term myocardial
infarction should not be used without further qualications,
whether in clinical practice, in the description of patient
cohorts, or in population studies. Such qualications should
refer to the amount of myocardial cell loss (infarct size), to
the circumstances leading to the infarct (e.g. spontaneous
or procedure related), and to the timing of the myocardial
necrosis relative to the time of the observation (evolving,
healing, or healed myocardial infarction).1
Following the 1999 ESC/ACC consensus conference, a
group of cardiovascular epidemiologists met to address the
specic needs of population surveillance. This international
meeting, representing several national and international
organizations, published recommendations in Circulation
2003.2 These recommendations addressed the needs of
researchers engaged in long-term population trend analysis
in the context of changing diagnostic tools using retrospec-
tive medical record abstraction. Also considered was surveil-
lance in developing countries and out-of-hospital death,
both situations with limited and/or missing data. These
recommendations continue to form the basis for epidemiolo-
gical research.
Given the considerable advances in the diagnosis and
management of myocardial infarction since the original
document was published, the leadership of the ESC, the
ACC, and the American Heart Association (AHA) convened,
together with the World Heart Federation (WHF), a Global
2527
Task Force to update the 2000 consensus document.1 As
with the previous consensus committee, the Global Task
Force was composed of a number of working groups in
order to rene the ESC/ACC criteria for the diagnosis of
myocardial infarction from various perspectives. With this
goal in mind, the working groups were composed of
experts within the eld of biomarkers, ECG, imaging, inter-
ventions, clinical investigations, global perspectives, and
implications. During several Task Force meetings, the rec-
ommendations of the working groups were co-ordinated,
resulting in the present updated consensus document.
The Task Force recognizes that the denition of myocar-
dial infarction will be subject to a variety of changes in
the future as a result of scientic advance. Therefore, this
document is not the nal word on this issue for all time.
Further renement of the present denition will doubtless
occur in the future.
Clinical features of ischaemia
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The term myocardial infarction reects cell death of
cardiac myocytes caused by ischaemia, which is the
result of a perfusion imbalance between supply and
demand. Ischaemia in a clinical setting most often can be
identied from the patients history and from the ECG.
Possible ischaemic symptoms include various combinations
of chest, upper extremity, jaw, or epigastric discomfort
with exertion or at rest. The discomfort associated with
acute myocardial infarction usually lasts at least 20 min.
Often, the discomfort is diffuse, not localized, not
positional, not affected by movement of the region, and
it may be accompanied by dyspnoea, diaphoresis, nausea,
or syncope.
These symptoms are not specic to myocardial ischaemia
and can be misdiagnosed and thus attributed to gastrointes-
tinal, neurological, pulmonary, or musculoskeletal dis-
orders. Myocardial infarction may occur with atypical
symptoms, or even without symptoms, being detected only
by ECG, biomarker elevations, or cardiac imaging.
Pathology
Myocardial infarction is dened by pathology as myocardial
cell death due to prolonged ischaemia. Cell death is cate-
gorized pathologically as coagulation and/or contraction
band necrosis, which usually evolves through oncosis, but
can result to a lesser degree from apoptosis. Careful analysis
of histological sections by an experienced observer is essen-
tial to distinguish these entities.1
After the onset of myocardial ischaemia, cell death is not
immediate but takes a nite period to develop (as little as
20 min or less in some animal models). It takes several
hours before myocardial necrosis can be identied by
macroscopic or microscopic post-mortem examination.
Complete necrosis of all myocardial cells at risk requires
at least 24 h or longer depending on the presence of collat-
eral circulation to the ischaemic zone, persistent or inter-
mittent coronary arterial occlusion, the sensitivity of the
myocytes to ischaemia, pre-conditioning, and/or, nally,
individual demand for myocardial oxygen and nutrients.
Myocardial infarctions are usually classied by size: micro-
scopic (focal necrosis), small [,10% of the left ventricular
(LV) myocardium], moderate (1030% of the LV
2528
myocardium), and large (.30% of the LV myocardium), and
by location. The pathological identication of myocardial
necrosis is made without reference to morphological
changes in the coronary arterial tree or to the clinical
history.1
Myocardial infarction can be dened pathologically as
acute, healing, or healed. Acute myocardial infarction is
characterized by the presence of polymorphonuclear leuko-
cytes. If the time interval between the onset of the infarc-
tion and death is quite brief, e.g. 6 h, minimal or no
polymorphonuclear leukocytes may be seen. The presence
of mononuclear cells and broblasts, and the absence of
polymorphonuclear leukocytes characterize healing infarc-
tion. Healed infarction is manifested as scar tissue without
cellular inltration. The entire process leading to a healed
infarction usually takes at least 56 weeks. Reperfusion
may alter the macroscopic and microscopic appearance of
the necrotic zone by producing myocytes with contraction
bands and large quantities of extravasated erythrocytes.
Myocardial infarctions can be classied temporally from
clinical and other features, as well as according to the
pathological appearance, as evolving (,6 h), acute (6 h7
days), healing (728 days), and healed (29 days and
beyond). It should be emphasized that the clinical and elec-
trocardiographic timing of the onset of an acute infarction
may not correspond exactly with the pathological timing.
For example, the ECG may still demonstrate evolving ST-T
changes and cardiac biomarkers may still be elevated
(implying a recent infarct) at a time when pathologically
the infarction is in the healing phase.1
Patients who suffer sudden cardiac death with or without
ECG changes suggestive of ischaemia represent a challen-
ging diagnostic group. Since these individuals die before
pathological changes can develop in the myocardium, it is
difcult to say with certainty whether these patients suc-
cumbed to a myocardial infarction or to an ischaemic
event that led to a fatal arrhythmia. The mode of death
in these cases is sudden, but the aetiology remains uncer-
tain unless the individual reported previous symptoms of
ischaemic heart disease prior to the cardiac arrest. Some
patients with or without a history of coronary disease may
develop clinical evidence of ischaemia, including prolonged
and profound chest pain, diaphoresis and/or shortness of
breath, and sudden collapse. These individuals may die
before blood samples for biomarkers can be obtained, or
these individuals may be in the lag phase before cardiac
biomarkers can be identied in the blood. These patients
may have suffered an evolving, fatal, acute myocardial
infarction. If these patients present with presumably new
ECG changes, for example ST elevation, and often with
symptoms of ischaemia, they should be classied as
having had a fatal myocardial infarction even if cardiac
biomarker evidence of infarction is lacking. Also, patients
with evidence of fresh thrombus by coronary angiography
(if performed) and/or at autopsy should be classied as
having undergone sudden death as a result of myocardial
infarction.
Clinical classication of myocardial infarction
Clinically the various types of myocardial infarction can be
classied as shown in Table 1.
K. Thygesen et al.
Table 1 Clinical classication of different types of myocardial
infarction
Type 1
Spontaneous myocardial infarction related to ischaemia due to
a primary coronary event such as plaque erosion and/or
rupture, ssuring, or dissection
Type 2
Myocardial infarction secondary to ischaemia due to either
increased oxygen demand or decreased supply, e.g. coronary
artery spasm, coronary embolism, anaemia, arrhythmias,
hypertension, or hypotension
Type 3
Sudden unexpected cardiac death, including cardiac arrest,
often with symptoms suggestive of myocardial ischaemia,
accompanied by presumably new ST elevation, or new LBBB, or
evidence of fresh thrombus in a coronary artery by angiography
and/or at autopsy, but death occurring before blood samples
could be obtained, or at a time before the appearance of
cardiac biomarkers in the blood
Type 4a
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Myocardial infarction associated with PCI
Type 4b
Myocardial infarction associated with stent thrombosis as
documented by angiography or at autopsy
Type 5
Myocardial infarction associated with CABG
On occasion, patients may manifest more than one type of
myocardial infarction simultaneously or sequentially. It
should also be noted that the term myocardial infarction
does not include myocardial cell death associated with
mechanical injury from coronary artery bypass grafting
(CABG), for example ventricular venting, or manipulation
of the heart; nor does it include myocardial necrosis due
to miscellaneous causes, e.g. renal failure, heart failure,
cardioversion, electrophysiological ablation, sepsis, myocar-
ditis, cardiac toxins, or inltrative diseases.
Biomarker evaluation
Myocardial cell death can be recognized by the appearance
in the blood of different proteins released into the circula-
tion from the damaged myocytes: myoglobin, cardiac tropo-
nin T and I, CK, LDH, as well as many others.3 Myocardial
infarction is diagnosed when blood levels of sensitive and
specic biomarkers such as cardiac troponin or CKMB are
increased in the clinical setting of acute myocardial ischae-
mia.1 Although elevations in these biomarkers reect myo-
cardial necrosis, they do not indicate its mechanism.3,4
Thus, an elevated value of cardiac troponin in the absence
of clinical evidence of ischaemia should prompt a search
for other aetiologies of myocardial necrosis, such as myocar-
ditis, aortic dissection, pulmonary embolism, congestive
heart failure, renal failure, and other examples indicated
in Table 2.
The preferred biomarker for myocardial necrosis is
cardiac troponin (I or T), which has nearly absolute myocar-
dial tissue specicity as well as high clinical sensitivity,
thereby reecting even microscopic zones of myocardial
necrosis.3 An increased value for cardiac troponin is
Universal denition of myocardial infarction
Table 2 Elevations of troponin in the absence of overt ischemic
heart disease
Cardiac contusion, or other trauma including surgery, ablation,
pacing, etc.
Congestive heart failureacute and chronic
Aortic dissection
Aortic valve disease
Hypertrophic cardiomyopathy
Tachy- or bradyarrhythmias, or heart block
Apical ballooning syndrome
Rhabdomyolysis with cardiac injury
Pulmonary embolism, severe pulmonary hypertension
Renal failure
Acute neurological disease, including stroke or subarachnoid
haemorrhage
Inltrative diseases, e.g. amyloidosis, haemochromatosis,
sarcoidosis, and scleroderma
Inammatory diseases, e.g. myocarditis or myocardial extension
of endo-/pericarditis
Drug toxicity or toxins
Critically ill patients, especially with respiratory failure or sepsis
Burns, especially if affecting .30% of body surface area
Extreme exertion
Modied from Jaffe et al.,4 and French and White.5
dened as a measurement exceeding the 99th percentile of
a normal reference population (URL upper reference
limit). Detection of a rise and/or fall of the measurements
is essential to the diagnosis of acute myocardial infarction.6
The above-mentioned discriminatory percentile is desig-
nated as the decision level for the diagnosis of myocardial
infarction, and must be determined for each specic assay
with appropriate quality control.79 Optimal precision [coef-
cient of variation (CV)] at the 99th percentile URL for each
assay should be dened as 10%. Better precision (CV 10%)
allows for more sensitive assays.10,11 The use of assays that
do not have independent validation of optimal precision
(CV10%) is not recommended. The values for the 99th per-
centile can be found on the International Federation for
Clinical Chemistry website http://www.ifcc.org/index.php?
option=com_remository&Itemid=120&func=leinfo&id=7.
Blood samples for the measurement of troponin should be
drawn on rst assessment (often some hours after the onset
of symptoms) and 69 h later.12 An occasional patient may
require an additional sample between 12 and 24 h if the
earlier measurements were not elevated and the clinical
suspicion of myocardial infarction is high.12 To establish
the diagnosis of myocardial infarction, one elevated value
above the decision level is required. The demonstration of
a rising and/or falling pattern is needed to distinguish back-
ground elevated troponin levels, e.g. patients with chronic
renal failure (Table 2), from elevations in the same patients
which are indicative of myocardial infarction.6 However, this
pattern is not absolutely required to make the diagnosis of
myocardial infarction if the patient presents .24 h after
the onset of symptoms. Troponin values may remain elev-
ated for 714 days following the onset of infarction.4
If troponin assays are not available, the best alternative is
CKMB (measured by mass assay). As with troponin, an
increased CKMB value is dened as a measurement above
the 99th percentile URL, which is designated as the decision
level for the diagnosis of myocardial infarction.9 Gender-
2529
specic values should be employed.9 The CKMB measure-
ments should be recorded at the time of the rst assessment
of the patient and 69 h later in order to demonstrate the
rise and/or fall exceeding the 99th percentile URL for the
diagnosis of myocardial infarction. An occasional patient
may require an additional diagnostic sample between 12
and 24 h if the earlier CKMB measurements were not elevated
and the clinical suspicion of myocardial infarction is high.
Measurement of total CK is not recommended for the diag-
nosis of myocardial infarction, because of the large skeletal
muscle distribution and the lack of specicity of this
enzyme.
Reinfarction
Traditionally, CKMB has been used to detect reinfarction.
However, recent data suggest that troponin values provide
similar information.13 In patients where recurrent myocar-
dial infarction is suspected from clinical signs or symptoms
following the initial infarction, an immediate measurement
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of the employed cardiac marker is recommended. A second
sample should be obtained 36 h later. Recurrent infarction
is diagnosed if there is a 20% increase of the value in the
second sample. Analytical values are considered to be
different if they are different by .3 SDs of the variance of
the measures.14 For troponin, this value is 57% for most
assays at the levels involved with reinfarction. Thus, a 20%
change should be considered signicant, i.e. over that
expected from analytical variability itself. This value
should also exceed the 99th percentile URL.
Electrocardiographic detection
of myocardial infarction
The ECG is an integral part of the diagnostic work-up
of patients with suspected myocardial infarction.1,2,15,16
The acute or evolving changes in the ST-T waveforms and
the Q-waves when present potentially allow the clinician
to date the event, to suggest the infarct-related artery,
and to estimate the amount of myocardium at risk. Coronary
artery dominance, size and distribution of arterial seg-
ments, collateral vessels, and location, extent, and severity
of coronary stenoses can also impact ECG manifestations of
myocardial ischaemia.17 The ECG by itself is often insuf-
cient to diagnose acute myocardial ischaemia or infarction
since ST deviation may be observed in other conditions
such as acute pericarditis, LV hypertrophy, LBBB, Brugada
syndrome, and early repolarization patterns.18 Also
Q-waves may occur due to myocardial brosis in the
absence of coronary artery disease, as in, for example,
cardiomyopathy.
ECG abnormalities of myocardial ischaemia
that may evolve to myocardial infarction
ECG abnormalities of myocardial ischaemia or infarction
may be inscribed in the PR segment, the QRS complex,
and the ST segment or T-waves. The earliest manifestations
of myocardial ischaemia are typical T-waves and ST segment
changes.19,20 Increased hyper-acute T-wave amplitude with
prominent symmetrical T-waves in at least two contiguous
leads is an early sign that may precede the elevation of
the ST segment. Increased R-wave amplitude and width
(giant R-wave with S-wave diminution) are often seen in
2530
Table 3 ECG manifestations of acute myocardial ischaemia
(in absence of LVH and LBBB)
ST elevation
New ST elevation at the J-point in two contiguous leads with
the cut-off points: 0.2 mV in men or 0.15 mV in women in
leads V2V3 and/or 0.1 mV in other leads
ST depression and T-wave changes
New horizontal or down-sloping ST depression 0.05 mV in two
contiguous leads; and/or T inversion 0.1 mV in two
contiguous leads with prominent R-wave or R/S ratio .1
leads exhibiting ST elevation, and tall T-waves reecting
conduction delay in the ischaemic myocardium.21 Transient
Q-waves may be observed during an episode of acute ischae-
mia or rarely during acute myocardial infarction with suc-
cessful reperfusion.22
Table 3 lists ECG criteria for the diagnosis of acute myo-
cardial ischaemia that may lead to infarction. The J-point
is used to determine the magnitude of the ST elevation.
J-point elevation in men decreases with increasing age;
however, that is not observed in women, in whom J-point
elevation is less than in men.23
Contiguous leads means lead groups such as anterior leads
(V1V6), inferior leads (II, III, and aVF), or lateral/apical
leads (I and aVL). More accurate spatial contiguity in the
frontal plane can be established by the Cabrera display:
aVL, I, aVR, II, aVF, and III.24 Supplemental leads such as
V3R and V4R reect the free wall of the right ventricle.
Although the criteria in Table 3 require that the ST shift be
present in two or more contiguous leads, it should be noted
that occasionally acute myocardial ischaemia may create
sufcient ST segment shift to meet the criteria in one lead
but have slightly less than the required ST shift in an adja-
cent contiguous lead. Lesser degrees of ST displacement or
T-wave inversion in leads without prominent R-wave ampli-
tude do not exclude acute myocardial ischaemia or evolving
myocardial infarction.
ST elevation or diagnostic Q-waves in regional lead groups
are more specic than ST depression in localizing the site of
myocardial ischaemia or necrosis.25,26 However, ST
depression in leads V1V3 suggests myocardial ischaemia,
especially when the terminal T-wave is positive (ST elevation
equivalent), and may be conrmed by concomitant ST
elevation 0.1 mV recorded in leads V7V9.27,28 The term
posterior to reect the basal part of the LV wall that lies
on the diaphragm is no longer recommended. It is preferable
to refer to this territory as inferobasal.29 In patients with
inferior myocardial infarction it is advisable to record right
precordial leads (V3R and V4R) seeking ST elevation in
order to identify concomitant right ventricular infarction.30
During an acute episode of chest discomfort, pseudo-
normalization of previously inverted T-waves may indicate
acute myocardial ischaemia. Pulmonary embolism, intracra-
nial processes, or peri-/myocarditis may also result in ST-T
abnormalities and should be considered (false positives) in
the differential diagnosis.
The diagnosis of myocardial infarction is difcult in the
presence of LBBB even when marked ST-T abnormalities or
ST elevation are present that exceed standard criteria.31,32
A previous ECG may be helpful to determine the presence
K. Thygesen et al.
Table 4 ECG changes associated with prior myocardial
infarction
Any Q-wave in leads V2V3 0.02 s or QS complex in leads V2
and V3
Q-wave 0.03 s and 0.1 mV deep or QS complex in leads I, II,
aVL, aVF, or V4V6 in any two leads of a contiguous lead
grouping (I, aVL,V6; V4V6; II, III, and aVF)a
R-wave 0.04 s in V1V2 and R/S 1 with a concordant positive
T-wave in the absence of a conduction defect
a
The same criteria are used for supplemental leads V7V9, and for the
Cabrera frontal plane lead grouping.
of acute myocardial infarction in this setting. In patients
with right bundle branch block (RBBB), ST-T abnormalities
in leads V1V3 are common, making it difcult to assess
the presence of ischaemia in these leads; however, when
ST elevation or Q-waves are found, myocardial ischaemia
or infarction should be considered. Some patients present
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with ST elevation or new LBBB, and suffer sudden cardiac
death before cardiac biomarkers become abnormal or
pathological signs of myocardial necrosis become evident
at autopsy. These patients should be classied as having
had a fatal myocardial infarction.
Prior myocardial infarction
As shown in Table 4, Q-waves or QS complexes in the
absence of QRS confounders are usually pathognomonic of
a prior myocardial infarction.3335 The specicity of the
ECG diagnosis for myocardial infarction is greatest when
Q-waves occur in several leads or lead groupings. ST devi-
ations or T-waves alone are non-specic ndings for myocar-
dial necrosis. However, when these abnormalities occur in
the same leads as the Q-waves, the likelihood of myocardial
infarction is increased. For example, minor Q-waves 0.02
and ,0.03 s that are 0.1 mV deep are suggestive of prior
infarction if accompanied by inverted T-waves in the same
lead group.
Other validated myocardial infarction-coding algorithms,
such as the Minnesota code, Novacode, and WHO MONICA,
dene Q-wave depth on the basis of depth, width, and
ratio of R-wave amplitude, such as Q-wave depth at least
one-third or one-fth of R-wave amplitude, and have been
used extensively in epidemiological studies and clinical
trials.36,37
Conditions that confound the ECG diagnosis
of myocardial infarction
A QS complex in lead V1 is normal. A Q-wave ,0.03 s and
,1/4 of the R-wave amplitude in lead III is normal if the
frontal QRS axis is between 30 and 08. The Q-wave may
also be normal in aVL if the frontal QRS axis is between 60
and 908. Septal Q-waves are small non-pathological
Q-waves ,0.03 s and ,1/4 of the R-wave amplitude in
leads I, aVL, aVF, and V4V6. Pre-excitation, obstructive or
dilated cardiomyopathy, LBBB, RBBB, left anterior hemi-
block, left and right ventricular hypertrophy, myocarditis,
acute cor pulmonale, or hyperkalaemia may be associated
with Q/QS complexes in the absence of myocardial infarc-
tion. ECG abnormalities that simulate myocardial ischaemia
or infarction are presented in Table 5.
Universal denition of myocardial infarction
Table 5 Common ECG pitfalls in diagnosing myocardial
infarction
False positives
Benign early repolarization
LBBB
Pre-excitation
Brugada syndrome
Peri-/myocarditis
Pulmonary embolism
Subarachnoid haemorrhage
Metabolic disturbances such as hyperkalaemia
Failure to recognize normal limits for J-point displacement
Lead transposition or use of modied MasonLikar
conguration24
Cholecystitis
False negatives
Prior myocardial infarction with Q-waves and/or persistent
ST elevation
Paced rhythm
LBBB
Reinfarction
The ECG diagnosis of reinfarction following the initial infarc-
tion may be confounded by the initial evolutionary ECG
changes. Reinfarction should be considered when ST
elevation 0.1 mV reoccurs in a patient having a lesser
degree of ST elevation or new pathognomonic Q waves, in
at least two contiguous leads, particularly when associated
with ischaemic symptoms for 20 min or longer. The
re-elevation of the ST segment can, however, also be seen
in threatening myocardial rupture and should lead to
additional diagnostic work-up. ST depression or LBBB on
their own should not be considered valid criteria for myocar-
dial infarction.
Coronary revascularization
ECG abnormalities during or after percutaneous coronary
intervention (PCI) are similar to those seen during spon-
taneous myocardial infarction. In patients who have under-
gone CABG, new ST-T abnormalities are common but not
necessarily diagnostic of myocardial ischaemia.38 However,
when new pathological Q waves (Table 4) appear in terri-
tories other than those identied before surgery, myocardial
infarction should be considered, particularly if associated
with elevated biomarkers, new wall motion abnormalities,
or haemodynamic instability.
Imaging techniques
Non-invasive imaging plays many roles in patients with
known or suspected myocardial infarction, but this section
concerns only its role in the diagnosis and characterization
of infarction. The underlying rationale is that regional myo-
cardial hypoperfusion and ischaemia lead to a cascade of
events including myocardial dysfunction, cell death, and
healing by brosis. Important imaging parameters are there-
fore perfusion, myocyte viability, myocardial thickness,
thickening, and motion, and the effects of brosis on the
kinetics of radiolabelled and paramagnetic contrast agents.
2531
Commonly used imaging techniques in acute and chronic
infarction are echocardiography, radionuclide ventriculogra-
phy, myocardial perfusion scintigraphy (MPS), and magnetic
resonance imaging (MRI). Positron emission tomography
(PET) and X-ray computed tomography (CT) are less
common. There is considerable overlap in their capabilities,
but only the radionuclide techniques provide a direct assess-
ment of myocardial viability because of the properties of the
tracers used. Other techniques provide indirect assessments
of myocardial viability, such as myocardial function from
echocardiography or myocardial brosis from MRI.
Echocardiography
Echocardiography is an excellent real-time imaging tech-
nique with moderate spatial and temporal resolution. Its
strength is the assessment of myocardial thickness, thicken-
ing, and motion at rest. This can be aided by tissue Doppler
imaging. Echocardiographic contrast agents can improve
endocardial visualization, but contrast studies are not yet
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fully validated for the detection of myocardial necrosis,
although early work is encouraging.39
Radionuclide imaging
Several radionuclide tracers allow viable myocytes to be
imaged directly, including thallium-201, technetium-99m
MIBI, tetrofosmin, and [18F]2-uorodeoxyglucose (FDG).4042
The strength of the techniques are that they are the only
commonly available direct methods of assessing viability,
although the relatively low resolution of the images disad-
vantages them for detecting small areas of infarction.43
The common single photon-emitting radio-pharmaceuticals
are also tracers of myocardial perfusion and so the tech-
niques readily detect areas of infarction and inducible per-
fusion abnormalities. ECG-gated imaging provides a
reliable assessment of myocardial motion, thickening, and
global function.44,45
Magnetic resonance imaging
Cardiovascular MRI has high spatial resolution and moderate
temporal resolution. It is a well-validated standard for the
assessment of myocardial function and has, in theory,
similar capability to echocardiography in suspected acute
infarction. It is, however, more cumbersome in an acute
setting and is not commonly used. Paramagnetic contrast
agents can be used to assess myocardial perfusion and the
increase in extracellular space associated with the brosis
of chronic infarction. The former is not yet fully validated
in clinical practice, but the latter is well validated and
can play an important role in the detection of
infarction.46,47
X-Ray computed tomography
Infarcted myocardium is initially visible to CT as a focal area
of decreased LV enhancement, but later imaging shows
hyperenhancement as with late gadolinium imaging by
MRI.48,49 This nding is clinically relevant because
contrast-enhanced CT may be performed for suspected
embolism and aortic dissection, conditions with clinical fea-
tures that overlap with those of acute myocardial infarction.
2532
Application in the acute phase
of myocardial infarction
Imaging techniques can be useful in the diagnosis of myocar-
dial infarction because of the ability to detect wall motion
abnormalities in the presence of elevated cardiac bio-
markers. If for some reason biomarkers have not been
measured or may have normalized, demonstration of new
loss of myocardial viability alone in the absence of non-
ischaemic causes meets the criteria for myocardial infarc-
tion. However, if biomarkers have been measured at appro-
priate times and are normal, the determinations of these
take precedence over the imaging criteria.
Echocardiography provides assessment of many non-
ischaemic causes of acute chest pain such as peri-myocarditis,
valvular heart disease, cardiomyopathy, pulmonary embolism,
or aortic dissection. Echocardiography is the imaging tech-
nique of choice for detecting complications of acute infarction
including myocardial free wall rupture, acute ventricular
septal defect, and mitral regurgitation secondary to papillary
muscle rupture or ischaemia. However, echocardiography
cannot distinguish regional wall motion abnormalities due to
myocardial ischaemia from infarction.
Radionuclide assessment of perfusion at the time of
patient presentation can be performed with immediate
tracer injection and imaging that can be delayed for up to
several hours. The technique is interpreter dependent,
although objective quantitative analysis is available. ECG
gating provides simultaneous information on LV function.
An important role of acute echocardiography or radio-
nuclide imaging is in patients with suspected myocardial
infarction and a non-diagnostic ECG. A normal echocardio-
gram or resting ECG-gated scintigram has a 9598% negative
predictive value for excluding acute infarction.5054 Thus,
imaging techniques are useful for early triage and discharge
of patients with suspected myocardial infarction.55,56
A regional myocardial wall motion abnormality or loss of
normal thickening may be caused by acute myocardial
infarction or by one or more of several other ischaemic con-
ditions including old infarction, acute ischaemia, stunning,
or hibernation. Non-ischaemic conditions such as cardiomyo-
pathy and inammatory or inltrative diseases can also lead
to regional loss of viable myocardium or functional abnorm-
ality, and so the positive predictive value of imaging tech-
niques is not high unless these conditions can be excluded
and unless a new abnormality is detected or can be pre-
sumed to have arisen in the setting of other features of
acute myocardial infarction.
Application in the healing or healed phase
of myocardial infarction
Imaging techniques are useful in myocardial infarction for
analysis of LV function, both at rest and during dynamic
exercise or pharmacological stress, to provide an assessment
of remote inducible ischaemia. Echocardiography and radio-
nuclide techniques, in conjunction with exercise or pharma-
cological stress, can identify ischaemia and myocardial
viability. Non-invasive imaging techniques can diagnose
healing or healed infarction by demonstrating regional wall
motion, thinning, or scar in the absence of other causes.
The high resolution of contrast-enhanced MRI means that
areas of late enhancement correlate well with areas of bro-
sis and thereby enable differentiation between transmural
K. Thygesen et al.
and subendocardial scarring.57 The technique is therefore
potentially valuable in assessing LV function and areas of
viable and hence potentially hibernating myocardium.
Myocardial infarction associated with
revascularization procedures
Peri-procedural myocardial infarction is different from spon-
taneous infarction, because the former is associated with the
instrumentation of the heart that is required during mechan-
ical revascularization procedures by either PCI or CABG. Mul-
tiple events that can lead to myocardial necrosis are taking
place, often in combination, during both types of interven-
tion.5861 While some loss of myocardial tissue may be una-
voidable during procedures, it is likely that limitation of
such damage is benecial to the patient and their prognosis.62
During PCI, myocardial necrosis may result from recogniz-
able peri-procedural events, alone or in combination, such
as side-branch occlusion, disruption of collateral ow,
distal embolization, coronary dissection, slow ow or
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no-reow phenomenon, and microvascular plugging. Emboli-
zation of intracoronary thrombus or atherosclerotic particu-
late debris cannot be entirely prevented despite current
antithrombotic and antiplatelet adjunctive therapy or pro-
tection devices. Such events induce extensive inammation
of non-infarcted myocardium surrounding small islets of
myocardium necrosis.6367 New areas of myocardial necrosis
have been demonstrated by MRI following PCI.68 A separate
subcategory of myocardial infarction is related to stent
thrombosis as documented by angiography and/or autopsy.
During CABG, numerous additional factors can lead to
peri-procedural necrosis. These include direct myocardial
trauma from sewing needles or manipulation of the heart,
coronary dissection, global or regional ischaemia related
to inadequate cardiac protection, microvascular events
related to reperfusion, myocardial damage induced by
oxygen free radical generation, or failure to reperfuse
areas of the myocardium that are not subtended by grafta-
ble vessels.6971 MRI studies suggest that most necrosis in
this setting is not focal, but diffuse and localized to the sub-
endocardium.72 Some clinicians and clinical investigators
have preferred using CKMB for the diagnosis of peri-
procedural infarction because of a substantial amount of
data relating CKMB elevations to prognosis.73,74 However,
an increasing number of studies using troponins in that
respect have emerged.59,75
Diagnostic criteria for myocardial infarction with PCI
In the setting of PCI, the balloon ination during a procedure
almost always results in ischaemia whether or not
accompanied by ST-T changes. The occurrence of
procedure-related cell necrosis can be detected by
measurement of cardiac biomarkers before or immediately
after the procedure, and again at 612 and 1824 h.76,77
Elevations of biomarkers above the 99th percentile URL
after PCI, assuming a normal baseline troponin value, are
indicative of post-procedural myocardial necrosis. There is
currently no solid scientic basis for dening a biomarker
threshold for the diagnosis of peri-procedural myocardial
infarction. Pending further data, and by arbitrary conven-
tion, it is suggested to designate increases more than
three times the 99th percentile URL as PCI-related myocar-
dial infarction (type 4a).
Universal denition of myocardial infarction
If cardiac troponin is elevated before the procedure and
not stable for at least two samples 6 h apart, there are insuf-
cient data to recommend biomarker criteria for the diag-
nosis of peri-procedural myocardial infarction.77 If the
values are stable or falling, criteria for reinfarction by
further measurement of biomarkers together with the fea-
tures of the ECG or imaging can be applied.
A separate subcategory of myocardial infarction (type 4b)
is related to stent thrombosis as documented by angiography
and/or autopsy. Although iatrogenic, myocardial infarction
type 4b with veried stent thrombosis must meet the cri-
teria for spontaneous myocardial infarction as well.
Diagnostic criteria for myocardial infarction
with CABG
Any increase of cardiac biomarkers after CABG indicates
myocyte necrosis, implying that an increasing magnitude of
biomarker is likely to be related to an impaired outcome.
This has been demonstrated in clinical studies employing
CKMB where elevations ve, 10 and 20 times the upper limit
of normal after CABG were associated with worsened progno-
sis.73,78,79 Likewise, the increase of troponin levels after CABG
indicates necrosis of myocardial cells, which predicts a poor
outcome, in particular when elevated to the highest quartile
or quintile of the troponin measurements.59,75
Unlike the prognosis, scant literature exists concerning
the use of biomarkers for dening myocardial infarction in
the setting of CABG. Therefore, biomarkers cannot stand
alone in diagnosing myocardial infarction (type 5). In view
of the adverse impact on survival observed in patients
with signicant biomarker elevations, this Task Force
suggests, by arbitrary convention, that biomarker values
more than ve times the 99th percentile of the normal
reference range during the rst 72 h following CABG, when
associated with the appearance of new pathological
Q-waves or new LBBB, or angiographically documented
new graft or native coronary artery occlusion, or imaging
evidence of new loss of viable myocardium, should be con-
sidered as diagnostic of a CABG-related myocardial infarc-
tion (type 5 myocardial infarction).
Table 6 Classication of the different types of myocardial infarction according to multiples of the 99th percentile URL of the applied
cardiac biomarker
Multiples  99% MI type 1 MI type 2 MI type 3*
(spontaneous) (secondary) (sudden death)
12 
23
35 
510 
.10 
Total number
*Biomarkers are not available for this type of myocardial infarction since the patients expired before biomarker determination could be performed.
**For the sake of completeness, the total distribution of biomarker values should be reported. The dark grey areas represent biomarker elevations below
the decision limit used for these types of myocardial infarction.
Irrespective of the specic end-point denition chosen in a clinical trial, all data should be provided. All boxes in the table should be completed, including
the shaded areas.
2533
Denition of myocardial infarction
in clinical investigations
A universal denition for myocardial infarction would be of
great benet to future clinical studies in this area since it
will allow for trial-to-trial comparisons as well as accurate
meta-analyses involving multiple investigations. In clinical
trials, myocardial infarction may be an entry criterion or
an end-point. The denition of myocardial infarction
employed in these trials will thus determine the character-
istics of patients entering the studies as well as the number
of outcome events. In recent investigations, different
infarct denitions have been employed, thereby hampering
comparison and generalization among these trials.
Consistency among investigators and regulatory auth-
orities with regard to the denition of myocardial infarction
used in clinical investigations is essential. The Task Force
strongly encourages trialists to employ the denition
described in this document. Furthermore, investigators
should ensure that a trial provides comprehensive data for
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the various types of myocardial infarction (e.g. spon-
taneous, peri-procedural) and includes the employed
decision limits for myocardial infarction of the cardiac bio-
markers in question. All data should be made available to
interested individuals in published format or on a website.
Data concerning infarctions should be available in a form
consistent with the current revised denitions of myocardial
infarction. This does not necessarily restrict trialists to a
narrow end-point denition, but rather ensures that across
all future trials access to comparable data exists, thereby
facilitating cross-study analyses. The recommendations put
forward in this section are not detailed and should be sup-
plemented by careful protocol planning and implementation
in any clinical trial.
The Task Force strongly endorses the concept of the same
decision limit for each biomarker employed for myocardial
infarction types 1 and 2, and, likewise, the same higher
three- and ve-fold decision limits in the setting of myocar-
dial infarction types 4a and 5, respectively7880 (Tables 6
and 7). In clinical trials, as in clinical practice, measurement
of cardiac troponin T or I is preferred over measurement of
CKMB or other biomarkers for the diagnosis of myocardial
MI type 4a** MI type 4b MI type 5** Total
(PCI) (stent thrombosis) (CABG) number
2534
Table 7 Sample clinical trial tabulation of randomized patients
by types of myocardial infarction
Types of MI Treatment A Treatment B
Number of patients Number of patients
MI type 1
MI type 2
MI type 3
MI type 4a
MI type 4b
MI type 5
Total number
infarction. Assessment of the quantity of myocardial damage
(infarct size) is also an important trial end-point. Although
the specic measurements vary depending on the assay
and whether cardiac troponin T or I is used, in most
studies troponin values correlate better with radionuclide-
and MRI-determined infarct size than do CK and CKMB.8183
The use of cardiac troponins will undoubtedly increase the
number of events recorded in a particular investigation
because of increased sensitivity for detecting infarction.8487
Ideally, data should be presented so that future clinical
investigations or registries can translate the myocardial
infarction end-point chosen in one study into the end-point
of another study. Thus, measurements should be presented
in a uniform manner to allow independent judgement and
comparison of the clinical end-points. Furthermore, this
Task Force suggests that data be reported as multiples of
the 99th percentile URL of the applied biomarker, enabling
comparisons between various classes and severity of the
different types of myocardial infarction as indicated in
Tables 6 and 7.
It is recommended that within a clinical trial all investi-
gators whenever possible should employ the same assay in
order to reduce the inter-assay variability, and, even
better, the latter could be reduced to zero by application
of a core laboratory using the same assay for all
measurements.
In the design of a study, investigators should specify the
expected effect of the new treatment under investigation.
Factors that should be considered include:
Assessment of the incidence of spontaneous myocardial
infarction (type 1) and infarction related to myocardial
oxygen supplies and demand (type 2) in treated patients
vs. control subjects.
Assessment of the incidence of sudden death related to
myocardial infarction when applying the suggested cri-
teria (type 3).
Assessment of the incidence of procedure-related myo-
cardial infarctions and biomarker elevations (PCI, types
4a and 4b; and CABG, type 5).
Public policy implications of redenition
of myocardial infarction
Evolution of the denition of a specic diagnosis such as
myocardial infarction has a number of implications for indi-
vidual citizens as well as for society at large. The process of
assigning a specic diagnosis to a patient should be
K. Thygesen et al.
associated with a specic value for the patient. The
resources spent on recording and tracking a particular diag-
nosis must also have a specic value to society in order to
justify the effort. A tentative or nal diagnosis is the basis
for advice about further diagnostic testing, treatment, life-
style changes, and prognosis for the patient. The aggregate
of patients with a particular diagnosis is the basis for health
care planning and policy, and resource allocation.
One of the goals of good clinical practice is to reach a
denitive and specic diagnosis, which is supported by
current scientic knowledge. The approach to the denition
of myocardial infarction outlined in this document meets
this goal. In general, the conceptual meaning of the term
myocardial infarction has not changed, although new sensi-
tive diagnostic methods have been developed to diagnose
this entity. Thus, the current diagnosis of acute myocardial
infarction is a clinical diagnosis based on patient symptoms,
ECG changes, and highly sensitive biochemical markers, as
well as information gleaned from various imaging tech-
niques. However, it is important to characterize the extent
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of the infarct as well as residual LV function and the severity
of coronary artery disease, rather than merely making a
diagnosis of myocardial infarction. The information con-
veyed about the patients prognosis and ability to work
requires more than just the mere statement that the
patient has suffered an infarct. The multiple other factors
just mentioned are also required so that appropriate
social, family, and employment decisions can be made.
A number of risk scores have been developed predicting
post-infarction prognosis. The classication of the various
other prognostic entities associated with myocardial necro-
sis should lead to a reconsideration of the clinical coding
entities currently employed for patients with the myriad
conditions that can lead to myocardial necrosis with conse-
quent elevation of biomarkers.
Many patients with myocardial infarction die suddenly.
Difculties in denition of sudden and out-of-hospital
death make attribution of the cause of death variable
among physicians, regions, and countries. For example,
out-of-hospital death is generally ascribed to ischaemic
heart disease in the USA but to stroke in Japan. These arbi-
trary and cultural criteria need re-examination.
It is important that any revised criteria for the denition
of myocardial infarction involve comparability of this de-
nition over time so that adequate trend data can be
obtained. Furthermore, it is essential to ensure widespread
availability and standard application of the measures in order
to ensure comparability of data from various geographic
regions. Shift in criteria resulting in a substantial increase
or decrease in case identication will have signicant
health resource and cost implications.86,87 Moreover, an
increase in sensitivity of the criteria for myocardial infarction
might entail negative consequences for some patients who
are not currently labelled as having had an infarction. On
the other hand, increasing diagnostic sensitivity for myocar-
dial infarction can have a positive impact for a society:
Increasing the sensitivity of diagnostic criteria for myo-
cardial infarction will result in more cases identied in a
society, thereby allowing appropriate secondary
prevention.
Increasing the specicity of diagnostic criteria for myo-
cardial infarction will result in more accurate diagnosis
Universal denition of myocardial infarction
but will not exclude the presence of coronary artery
disease, the cases of which may benet from secondary
prevention.
It should be appreciated that the agreed modication of the
denition of myocardial infarction may be associated with
consequences for the patients and their families with
respect to psychological status, life insurance, professional
career, as well as driving and pilot licences. Also the diagnosis
is associated with societal implications as to diagnosis-
related coding, hospital reimbursement, mortality stat-
istics, sick leave, and disability attestation.
In order to meet this challenge, physicians must be
adequately informed of the altered diagnostic criteria.
Educational materials will need to be created and treatment
guidelines must be appropriately adapted. Professional
societies should take steps to facilitate the rapid dissemina-
tion of the revised denition to physicians, other health care
professionals, administrators, and the general public.
Global perspectives of the redenition
of myocardial infarction
Cardiovascular disease is a global health problem. Approxi-
mately one-third of persons in the world die of cardiovascu-
lar disease, largely coronary artery disease and stroke, and
80% of these deaths from cardiovascular disease occur in
developing countries. The greater proportion of deaths is
due to heart disease and specically coronary heart
disease, of which myocardial infarction is a major manifes-
tation. Since it is difcult to measure the prevalence of cor-
onary artery disease in a population, the incidence of
myocardial infarction may be used as a proxy, provided
that a consistent denition is used when different popu-
lations, countries, or continents are being compared.
The changes in the denition of myocardial infarction
have critical consequences for less developed and develop-
ing countries. In many countries, the resources to apply
the new denition may not be available in all hospitals.
However, many developing countries already do have
medical facilities capable of or currently employing the pro-
posed denition of myocardial infarction. In the context of
the overall cost for a patient with myocardial infarction,
the expense associated with a troponin assay would not be
excessive and should be economically affordable in many
hospitals in developing countries, particularly those where
infarcts are frequent events. The necessary equipment,
staff training, and running costs may be lacking in some
regions, but certainly not in others. In less advantaged hos-
pitals, the diagnosis of myocardial infarction may depend
mostly on clinical signs and symptoms coupled with less
sophisticated biomarker analyses. Some of these institutions
may only have access to CK and its isoenzymes at the
The CME Text Universal denition of myocardial infarction is accredited by the European Board for Accreditation in Cardiology (EBAC) for 1 hour of external CME credits.
Each participant should claim only those hours of credit that have actually been spent in the educational activity. EBAC works according to the quality standards of the Euro-
pean Accreditation Council for Continuing Medical Education (EACCME), which is an institution of the European Union of Medical Specialists (UEMS). In compliance with EBAC/
EACCME guidelines, all authors participating in this programme have disclosed potential conicts of interest that might cause a bias in the article. The Organizing Committee
is responsible for ensuring that all potential conicts of interest relevant to the programme are declared to the participants prior to the CME activities.
CME questions for this article are available at: European Heart Journal http://cme.oxfordjournals.org/cgi/hierarchy/oupcme_node;ehj and European Society of Cardiol-
ogy http://www.escardio.org/knowledge/guidelines.
2535
present time. The redenition arises from and is compatible
with the latest scientic knowledge and with advances in
technology, particularly with regard to the use of bio-
markers, high quality electrocardiography, and imaging
techniques. The denition can and should be used by devel-
oped countries immediately, and by developing countries as
quickly as resources become available.
The change in the denition of myocardial infarction will
have a substantial impact on the identication, prevention,
and treatment of cardiovascular disease throughout the
world. The new denition will impact epidemiological data
from developing countries relating to prevalence and inci-
dence. The simultaneous and continuing use of the older
WHO denition for some years would allow a comparison
between data obtained in the past and data to be acquired
in the future employing the newer biomarker approach.
Cultural, nancial, structural, and organizational problems
in the different countries of the world in diagnosis and
therapy of acute myocardial infarction will require on-
going investigation. It is essential that the gap between
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therapeutic and diagnostic advances be addressed in this
expanding area of cardiovascular disease.
Conicts of interest
The members of the Task Force established by the ESC, the ACCF,
AHA and the WHF have participated independently in the pre-
paration of this document, drawing on their academic and clinical
experience and applying an objective and critical examination of
all available literature. Most have undertaken and are undertaking
work in collaboration with industry and governmental or private
health providers (research studies, teaching conferences, consul-
tation), but all believe such activities have not inuenced their
judgement. The best guarantee of their independence is in the
quality of their past and current scientic work. However, to
ensure openness, their relations with industry, government and
private health providers are reported in the ESC and European
Heart Journal websites (www.escardio.org and www.eurheartj.org).
Expenses for the Task Force/Writing Committee and preparation of
this document were provided entirely by the above mentioned joint
associations.
Acknowledgements
We are indebted to Professor Erling Falk MD for reviewing the
section on Pathology. Furthermore, we are very grateful to the
dedicated staff of the Guidelines Department of the ESC. We
would also like to thank and to acknowledge the contribution of
the following companies through unrestricted educational grants,
none of whom were involved in the development of this publication
and in no way inuenced its contents. Premium observer: GSK.
Observer: AstraZeneca, Beckman-Coulter, Dade Behring, Roche
Diagnostics, Sano-Aventis, Servier.
2536
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